Nerve insensitivity resistance to synthetic pyrethroids was detected in a resistant ®eld strain (JSFX-R) of the cotton bollworm, Helicoverpa armigera (Hu È bner), using a neurophysiological assay in which extracellular spontaneous neuronal activity was measured in response to cis-cypermethrin. The nerve insensitivity mechanism was selected using a combination of toxicological and neurophysiological methods. The third-instar larvae in selected strains of Family-37 and CTR strain expressed a very high resistance to fenvalerate (RF = 2060-fold and 805-fold, respectively) and high cross-resistance to DDT (RF = 1927-fold and 2384-fold, respectively) which was not affected by two metabolic synergists, PBO and DMC. The frequency of nerve-insensitive individuals detected in neurophysiological assays (54, 81 and 100% for JSFX-R strain, and the selected strains Family-43 and Family-37, respectively) was not only positively correlated (R 2 = 0.968) with the frequency of non-PBOsynergisable resistant individuals detected in toxicological tests (37.5, 62.5 and 90% for JSFX-R strain, Family-43 and Family-37, respectively), but also positively correlated (R 2 = 0.978) with the frequency of DDT-resistant individuals detected in toxicological tests (40, 67.5 and 93.3% for JSFX-R strain, Family-43 and Family-37, respectively). Analysis of dose±mortality lines to DDT and fenvalerate from F 1 hybrids (R, Â S<) indicated that nerve insensitivity resistance to DDT and fenvalerate in the CTR strain was inherited in an incompletely recessive pattern. Degree of dominance (D) was estimated to be À0.66 (AE 0.06) (DDT) and À0.26 (AE 0.04) (fenvalerate). The dose±mortality curves to DDT in backcross progeny were strongly suggested, by chi-square analysis, to be ®tted with those expected of a onegene model. Evidence for the co-existence of nerve insensitivity and oxidative metabolic resistance mechanisms within individual H armigera and the effects of their interaction on the expression of resistance to fenvalerate are discussed.